alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–25 of 566 studies in Lewy body dementia (page 1 of 23) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

What “Lewy body dementia” covers

Lewy body dementia — Dementia with Lewy bodies and related conditions: how they differ from Alzheimer's in symptoms, diagnosis and care.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

A clinico-pathological study of subtypes in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Brain : a journal of neurology 2009-09-16

We have carried out a systematic review of the case files of 242 donors with pathologically verified Parkinson's disease at the Queen Square Brain Bank for Neurological Disorders in an attempt to corroborate the data-driven subtype classification proposed by Lewis and colleagues (Heterogeneity of Parkinson's disease in the early clinical stages using a data driven approach. 4 key findings →

Design: systematic review Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Comparison of risperidone and placebo for psychosis and behavioral disturbances associated with dementia: a randomized, double-blind trial. Risperidone Study Group

✓ Peer-reviewed alzhub usefulness score 68 out of 100. The Journal of clinical psychiatry 1999-02-01

The study was completed by 70% of the patients. 4 key findings →

Participants: 625 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Identifying dementia outcomes in UK Biobank: a validation study of primary care, hospital admissions and mortality data

✓ Peer-reviewed alzhub usefulness score 66 out of 100. European journal of epidemiology 2019-02-26

Prospective, population-based studies that recruit participants in mid-life are valuable resources for dementia research. 1 key finding →

Participants: 500,000 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 65 out of 100. PLoS genetics 2008-09-19

The TAR DNA-binding protein 43 (TDP-43) has been identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin inclusions (FTLD-U), defining a novel class of neurodegenerative conditions: the TDP-43 proteinopathies. 3 key findings →

Participants: 296 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

The effect of Lewy body (co-)pathology on the clinical and imaging phenotype of amnestic patients

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Brain 2025-01-31

Based on positive/negative results on the different biomarkers, subjects were classified as 'AD-LB-' (n = 304), 'AD+LB-' (n = 335), 'AD+LB+' (n = 158) and 'AD-LB+' (n = 68). 5 key findings →

Design: longitudinal study Participants: 661 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 1998-06-01

Thirteen families have been described with an autosomal dominantly inherited dementia named frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), historically termed Pick's disease. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease: a practical approach

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Acta neuropathologica 2011-11-20

We present a practical guide for the implementation of recently revised National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease (AD). 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Null mutations in progranulin cause ubiquitin-positive frontotemporal dementia linked to chromosome 17q21

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2006-07-16

Frontotemporal dementia (FTD) with ubiquitin-immunoreactive neuronal inclusions (both cytoplasmic and nuclear) of unknown nature has been linked to a chromosome 17q21 region (FTDU-17) containing MAPT (microtubule-associated protein tau). 5 key findings →

Participants: 17 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature medicine 2020-03-02

With the potential development of new disease-modifying Alzheimer's disease (AD) therapies, simple, widely available screening tests are needed to identify which individuals, who are experiencing symptoms of cognitive or behavioral decline, should be further evaluated for initiation of treatment. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

TDP-43 represses cryptic exon inclusion in the FTD-ALS gene UNC13A

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2022-02-23

A hallmark pathological feature of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the depletion of RNA-binding protein TDP-43 from the nucleus of neurons in the brain and spinal cord 1 . 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2022-02-23

Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia 1-3 , two related neurodegenerative diseases defined by mislocalization of the RNA-binding protein TDP-43 4,5 . 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Genome-wide association meta-analysis of neuropathologic features of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 64 out of 100. PLoS genetics 2014-09-04

Alzheimer's disease (AD) and related dementias are a major public health challenge and present a therapeutic imperative for which we need additional insight into molecular pathogenesis. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neuron 2011-09-21

The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2012-01-01

A consensus panel from the United States and Europe was convened recently to update and revise the 1997 consensus guidelines for the neuropathologic evaluation of Alzheimer's disease (AD) and other diseases of brain that are common in the elderly. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Decreased synaptic proteins in neuronal exosomes of frontotemporal dementia and Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 63 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2016-09-06

Synaptic dysfunction occurs early in senile dementias, presumably as a result of decreased levels of functional synaptic proteins as found in autopsied brains of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD). 3 key findings →

Design: cross-sectional Participants: 12 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Shared and disease-specific pathways in frontotemporal dementia and Alzheimer’s and Parkinson’s diseases

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Nature Medicine 2025-07-15

Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and frontotemporal dementia (FTD), exhibit distinct yet overlapping pathological mechanisms. 2 key findings →

Participants: 10,527 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Sex differences in the clinical manifestation of autosomal dominant frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Alzheimer s & Dementia 2025-04-01

While sex differences were not apparent at asymptomatic stages, females showed more rapid declines across all outcomes in symptomatic stages compared to males. 5 key findings →

Design: longitudinal study Participants: 337 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Increased plasma DOPA decarboxylase levels in Lewy body disorders are driven by dopaminergic treatment

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Nature Communications 2025-01-29

DOPA Decarboxylase (DDC) has been proposed as a cerebrospinal fluid (CSF) biomarker with increased concentrations in Lewy body disorders (LBDs) and highest levels in patients receiving dopaminergic treatment. 2 key findings →

Design: longitudinal study Participants: 71 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

↑ Change the filters

Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed